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Relationship between clopidogrel-induced platelet P2Y12 inhibition and stent thrombosis or myocardial infarction after percutaneous coronary intervention-A case-control study

Varenhorst, Christoph; Koul, Sasha LU ; Erlinge, David LU ; Lagerqvist, Bo; Siegbahn, Agneta; Wallentin, Lars and James, Stefan (2011) In American Heart Journal 162(2). p.363-371
Abstract
Background Insufficient platelet inhibition is a major determinant of stent thrombosis (STh), although the etiology is multifactorial. On-clopidogrel platelet reactivity was investigated in patients with previous angiographically confirmed STh, myocardial infarction (MI), and controls. Methods Using the Swedish Coronary Angiography and Angioplasty Registry, we identified patients with angiographically confirmed STh (n = 48) or MI (n = 30) while on dual antiplatelet therapy within 6 months of percutaneous coronary intervention (PCI) and matched control patients (n = 78). On-clopidogrel platelet reactivity was measured with VerifyNow P2Y12 and vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay. Results The mean P2Y12 reaction... (More)
Background Insufficient platelet inhibition is a major determinant of stent thrombosis (STh), although the etiology is multifactorial. On-clopidogrel platelet reactivity was investigated in patients with previous angiographically confirmed STh, myocardial infarction (MI), and controls. Methods Using the Swedish Coronary Angiography and Angioplasty Registry, we identified patients with angiographically confirmed STh (n = 48) or MI (n = 30) while on dual antiplatelet therapy within 6 months of percutaneous coronary intervention (PCI) and matched control patients (n = 78). On-clopidogrel platelet reactivity was measured with VerifyNow P2Y12 and vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay. Results The mean P2Y12 reaction units (PRU) was higher (246.8 +/- 75.9 vs 200.0 +/- 82.7, P = .001) in STh patients compared with controls. The optimal cutoff for STh was 222 PRU or higher (area under the curve 0.69, P < .0001) in a receiver operating characteristics (ROC) analysis. The cutoff level resulted in 70.2% sensitivity and 67.3% specificity. There was no significant difference in mean PRU but a higher device-reported percent inhibition (45.1 +/- 23.8 vs 32.1 +/- 23.2, P = .04) in patients with MI compared with controls. Results with the VASP phosphorylation assay were not related to the occurrence of STh or MI. Conclusions STh was associated with high on-clopidogrel platelet reactivity measured with VerifyNow (cutoff level of PRU = 222) but spontaneous MI in stented patients on clopidogrel treatment was not. There was, however, a substantial overlap in on-clopidogrel platelet reactivity between patients with and without on-treatment STh questioning the clinical use of platelet function testing to identify patients at high risk for STh. (Am Heart J 2011;162:363-71.) (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
American Heart Journal
volume
162
issue
2
pages
363 - 371
publisher
Mosby
external identifiers
  • wos:000293729400021
  • scopus:80051666852
ISSN
1097-6744
DOI
10.1016/j.ahj.2011.06.003
language
English
LU publication?
yes
id
17051be9-7961-42c1-aabb-6f34f72de175 (old id 2163041)
date added to LUP
2011-10-03 08:39:19
date last changed
2017-01-01 03:13:10
@article{17051be9-7961-42c1-aabb-6f34f72de175,
  abstract     = {Background Insufficient platelet inhibition is a major determinant of stent thrombosis (STh), although the etiology is multifactorial. On-clopidogrel platelet reactivity was investigated in patients with previous angiographically confirmed STh, myocardial infarction (MI), and controls. Methods Using the Swedish Coronary Angiography and Angioplasty Registry, we identified patients with angiographically confirmed STh (n = 48) or MI (n = 30) while on dual antiplatelet therapy within 6 months of percutaneous coronary intervention (PCI) and matched control patients (n = 78). On-clopidogrel platelet reactivity was measured with VerifyNow P2Y12 and vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay. Results The mean P2Y12 reaction units (PRU) was higher (246.8 +/- 75.9 vs 200.0 +/- 82.7, P = .001) in STh patients compared with controls. The optimal cutoff for STh was 222 PRU or higher (area under the curve 0.69, P &lt; .0001) in a receiver operating characteristics (ROC) analysis. The cutoff level resulted in 70.2% sensitivity and 67.3% specificity. There was no significant difference in mean PRU but a higher device-reported percent inhibition (45.1 +/- 23.8 vs 32.1 +/- 23.2, P = .04) in patients with MI compared with controls. Results with the VASP phosphorylation assay were not related to the occurrence of STh or MI. Conclusions STh was associated with high on-clopidogrel platelet reactivity measured with VerifyNow (cutoff level of PRU = 222) but spontaneous MI in stented patients on clopidogrel treatment was not. There was, however, a substantial overlap in on-clopidogrel platelet reactivity between patients with and without on-treatment STh questioning the clinical use of platelet function testing to identify patients at high risk for STh. (Am Heart J 2011;162:363-71.)},
  author       = {Varenhorst, Christoph and Koul, Sasha and Erlinge, David and Lagerqvist, Bo and Siegbahn, Agneta and Wallentin, Lars and James, Stefan},
  issn         = {1097-6744},
  language     = {eng},
  number       = {2},
  pages        = {363--371},
  publisher    = {Mosby},
  series       = {American Heart Journal},
  title        = {Relationship between clopidogrel-induced platelet P2Y12 inhibition and stent thrombosis or myocardial infarction after percutaneous coronary intervention-A case-control study},
  url          = {http://dx.doi.org/10.1016/j.ahj.2011.06.003},
  volume       = {162},
  year         = {2011},
}